PM2.5-Induced Oxidative Stress and Mitochondrial Damage in the Nasal Mucosa of Rats
Open accessAbstract
Exposure to PM2.5 (particulate matter ≤2.5 μm) increases the risk of nasal lesions, but the underlying mechanisms, especially the mechanisms leading to mitochondrial damage, are still unclear. Thus, we investigated the in vivo effects of PM2.5 exposure on the inflammatory response, oxidative stress, the enzyme activities of Na+K+-ATPase and Ca2+-ATPase, and the morphology and function of mitochondria in the nasal mucosa of rats. Exposure to PM2.5 occurred through inhalation of a PM2.5 solution aerosol. The results show that the PM2.5 exposure induced increased levels of malondialdehyde (MDA) and levels of proinflammatory mediators, including interleukin 6 (IL-6), IL-8, and tumor necrosis factor-α (TNF-α). These changes were accompanied by decreases in the activities of total superoxide dismutase (T-SOD), Na+K+-ATPase, and Ca2+-ATPase in rat nasal mucosa. PM2.5 significantly affected the expression of specific mitochondrial fission/fusion genes (OPA1, Mfn1, Fis1, and Drp1) in nasal mucosa. These changes were accompanied by abnormal alterations of mitochondrial structures, including mitochondrial swelling, cristae disorder, and even fission resulting from higher doses of PM2.5. Our data shows that oxidative damage, inflammatory response, and mitochondrial dysfunction may be the toxic mechanisms that cause nasal lesions after exposure to PM2.5.
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Mitochondria are targeted by environmental pollutants such as PM2.5.
“Mitochondria are targeted by environmental pollutants such as PM2.5 (Guo et al. 2017)”
From Particulate matter 2.5 damages skin cells by inducing oxidative stress, subcellular organelle dysfunction, and apoptosis (2018) · cites this paper as Guo et al. 2017
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- Authors
- Guo, Z., Hong, Z., Dong, W., Deng, C., Zhao, R., Xu, J., Zhuang, G., & Zhang, R.
- Affiliations
- Fudan University (CN)
- Corresponding author
- Zhang, Ruxin
- Venue
- International Journal of Environmental Research and Public Health
- Publisher
- MDPI AG
- Published
- 2017-01-29
- Volume
- 14
- Issue
- 2
- Pages
- 134
- ISSN
- 1660-4601 (ISSN-L)
- PMC
- PMC5334688
- OpenAlex
- W2582797467
- Cited by
- 119
- References
- 22
- Citations by year
- 2026: 9 · 2025: 16 · 2024: 11 · 2023: 15 · 2022: 15 · 2021: 17 · 2020: 15 · 2019: 9 · 2018: 7 · 2017: 5
- FWCI
- 5.31
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- International Journal of Environmental Research and Public Health (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- Funders
- The National Natural Science Foundation of China (Grant No. 81371078)
- Topics
- Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Air Quality and Health Impacts
- Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Indoor Air Quality and Microbial Exposure
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Keywords
- PM2.5, particulate matter, nasal mucosa, oxidative stress, mitochondrial damage, mitochondrial fission and fusion, mitochondrial dysfunction, air pollution toxicity, inflammation, Na+/K+-ATPase, Ca2+-ATPase, superoxide dismutase, malondialdehyde, OPA1, Mfn1, Fis1, Drp1, nasal lesions
- MeSH terms
- Air Pollutants, Animals, Disease Models, Animal, Female, Inflammation, Malondialdehyde, Mitochondria, Nasal Mucosa, Particle Size, Tumor Necrosis Factor-alpha, Interleukin-6, Interleukin-8, Oxidative Stress, Mitochondrial Proteins, Rats, Particulate Matter
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